Most strains of mice are unable to make an antibody response to poly(glu50tyr50) (GT). In some strains, this unresponsiveness is due to the development of antigen-specific suppressor T cells and specific suppressor factor(s) which arise following GT injection. Pretreatment of suppressor mice with cyclophosphamide (CY) previous to GT injection eliminates the suppressive effect. Preliminary studies show that GT-specific helper T cells and helper factor(s) arise in these CY-treated GT-primed mice. Administration of helper factor(s) derived from CY-treated, GT-primed mice to normal, untreated GT-suppressor mice allows these recipient mice to make an antibody response to GT challenge. The basis for GT-nonsuppressor strains of mice inability to respond to GT challenge is not entirely clear. We propose to direct the activities of our laboratory to two major goals: a) Determination of the underlying cause(s) for GT-unresponsiveness in 'GT-nonsuppressor' strains of mice. b) Functional characterization of GT-specific helper cells and factor(s).